Relative risk of cardiovascular morbidity is increased in Chronic Kidney Disease (CKD). According to current KDIGO guideline cardiovascular risk can be estimated from Glomerular Filtration Rate (GFR) and proteinuria.

1. Short Communication
High Sensitive Troponin T has an
Incremental Value in Estimation of
Cardiovascular Risk in Chronic Kidney
Disease -
Anna V. Olah1
*, Timea Szalko2
, Eszter Szantho1
, Eva Varga3
, Janos
Matyus4
, Jozsef Varga5
1
Department of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary
2
Fejér County Hospital, Székesfehérvár, Hungary
3
3rd
Department of Internal Medicine, Semmelweis University, Budapest, Hungary
4
Department of Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary
5
Department of Medical Imaging, Faculty of Medicine, University of Debrecen, Debrecen, Hungary
*Address for Correspondence: Anna V. Olah, Department of Laboratory Medicine, Faculty of Medicine,
University of Debrecen, Nagyerdei krt 98, H-4032 Debrecen, Hungary, E-mail: olaha@med.unideb.hu
Submitted: 12 December 2016; Approved: 29 December 2016; Published: 27 January 2017
Citation this article: Olah AV, Szalko T, Szantho E, Varga E, Matyus J, et al. High Sensitive Troponin
T has an Incremental Value in Estimation of Cardiovascular Risk in Chronic Kidney Disease. Int J
Nephrol Ther. 2017;3(1): 001-006.
Copyright: © 2016 Olah AV, et al. This is an open access article distributed under the Creative
Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any
medium, provided the original work is properly cited.
International Journal of
Nephrology & Therapeutics

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Abbreviations
ACR: Urinary Albumin/Creatinine Ratio; CKD: Chronic Kidney
Disease; GFR-EPI: estimated Glomerular Filtration Rate published by
CKD-Epidemiology Collaboration; hsTnT: High Sensitive Troponin
T; HbA1c: Hemoglobin A1c; non–HDL-C: difference between total
cholesterol and HDL-cholesterol; Scr: Serum Creatinine; TPCR:
Urinary Total Protein/Creatinine
Introduction
Cardiovascular mortality risk is increased in all stages of chronic
kidney disease [1-4]. Although cardiac troponin is the first choice in
the diagnosis of acute myocardial infarction, proper interpretation
of slightly elevated troponin is challenging, because high sensitive
troponin T tests applied since ~2009 detect even the smallest cardiac
damage. Recent clinical studies proved that high sensitive troponin
level depends on GFR, and it increases with the impairment of renal
function. According to the current KDIGO 2013 guideline [5],
automatedreportingofestimatedGlomerularFiltrationRate(GFR)in
laboratories established the classification of Chronic Kidney Disease
(CKD). However, recognition of chronic kidney disease in early stage
is often based on albuminuria or proteinuria [6-15]. According to
KDIGO 2013 guideline for the assessment of cardiovascular risk in
chronic kidney disease GFR- and proteinuria-based renal score is
recommended.
The first aim of this study was to evaluate whether renal score
is enough to estimate cardiovascular risk in CKD for a long run.
Therefore, in Study A we retrospectively evaluated renal scores,
GFR, proteinuria and the effect of proteinuria on the efficacy of lipid
lowering therapy during a four-year period.
The second aim was to prove whether high sensitive troponin T
(hsTnT) has an incremental value to predict cardiovascular risk. For
this we evaluated hsTnT at different stages of CKD and correlation
with clinical cardiovascular score (Study B). As the permanently
elevated hsTnT is common in CKD, correct evaluation of cardiac
state is a crucial task at emergency departments, nephrology or
cardiac centers.
Subjects and Methods
Study A
First in a retrospective study we reviewed the clinical and
laboratory data of 400 patients, who were followed regularly at the
Nephrology Outpatient Centre, University of Debrecen in a four-
year period (2009-2012) without acute cardiac events. To calculate
Framingham clinical cardiovascular scores and renal scores, we could
enroll only 20 patients who had a complete medical history (Table 1)
and all laboratory results (serum creatinine, GFR, urinary protein (or
albumin), creatinine from the first morning urine, serum cholesterol,
LDL-C, HDL-C, triglyceride and HbA1c in diabetes mellitus) each
year (2009-2012). At the beginning of Study A median age of the 20
patients (15 men, 5 women) was 65 years (38-88 years). The clinical
score indicating the risk of cardiovascular mortality was estimated
from the parameters of the Framingham study [16,17]. The patient’s
history and traditional cardiovascular risk markers were taken into
account as it is detailed in Table 1 (age, BMI, blood pressure, cardiac
events, myocardial infarction, stroke, blood lipids, hyperglycemia,
diabetes mellitus, HbA1c). Renal score was estimated from the
glomerular filtration rate (GFR-EPI) and urinary protein/creatinine
or albumin/creatinine ratio (Table 2). The patients were sorted into
four groups of severity based on renal scores (1: low, 2: moderate,
3: high, 4: extremely high cardiovascular risk). The advantage of
GFR-EPI formula is the reliability up to 90 ml/min/1.73 m2
; it was
calculated as Levey et al published for adults in 2009 [14]:
Female if Scr <62 µmol/ L: eGFR=144×(Scr/61.6)–0,329
×(0.993) age
Female if Scr >62 µmol/ L: eGFR=144×(Scr/61.6)–1,209
×(0.993) age
Male if Scr <80 µmol/ L: eGFR=141×(Scr/79.2)–0,411
×(0.993) age
Male if Scr >80 µmol/ L: eGFR=141×(Scr/79.2)–1,209
×(0.993)age
Fasting blood samples were collected in Becton-Dickinson
vacuum tubes with a gel separator. After centrifugation (1800 g, 10
min) clinical biochemical tests were performed on a Cobas-6000
analyzer (Roche Diagnostics Ltd, Mannheim). Serum cholesterol and
triglyceride were determined by enzymatic assay, HDL-cholesterol
Abstract
Relative risk of cardiovascular morbidity is increased in Chronic Kidney Disease (CKD). According to current KDIGO guideline
cardiovascular risk can be estimated from Glomerular Filtration Rate (GFR) and proteinuria.
Aims: First aim was to evaluate renal score, is it enough to estimate cardiovascular risk in CKD. Then we checked whether high
sensitive Troponin T (hsTnT) has an incremental value to predict cardiovascular risk in CKD.
Methods: Clinical cardiovascular score was established according to the Framingham study: age, BMI, blood pressure, lipids, patient
history (diabetes mellitus, myocardial infarction, stroke). Renal severity scores (1-4) were determined from GFR and urinary albumin/
creatinine or protein/creatinine. Biochemical parameters were determined by Cobas 6000.
Results: Results in Study A (n:20) Mean of GFR decreased (66 ± 12 vs. 47 ± 16 ml/min/1.73 m2
) and renal score impaired (2.5 ±
1.1 vs. 3 ± 0.9) during four years. Clinical cardiovascular score was proportional to the renal score: clinical score was 21.8 ± 9.8 at renal
score <3.5 and 29.2 ± 6.7 at renal score >3.5 (p:0.09). Proteinuria has prognostic value in lipid lowering therapy: atherogenic non-HDL
was reducible from 3.62 ± 0.75 to 2.92 ± 0.63 mmol/ L without proteinuria. In Study B (n:21) mean of clinical cardiovascular score was
21.5 ± 2.1 at moderate renal damage and 27.4 ± 9.2 at severe renal damage. Mean of hsTnT was also lower (14.8 ± 11.3) at renal scores
1-2 compared to hsTnT (32.8 ± 20.9 ng/ L) at renal scores 3-4. Individual hsTnT correlated with clinical scores (R = 0.655, P < 0.001).
Conclusions: Impairment of renal score indicates higher cardiovascular risk. Permanent moderate elevation of hsTnT refers to
increased cardiovascular risk, which has incremental value in the treatment of CKD.
Keywords: Cardiovascular mortality; Glomerular filtration rate; Proteinuria; Renal score; Troponin

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and LDL-cholesterol were measured by homogenous enzymatic
assay. For monitoring the efficacy of lipid lowering therapy, non-
HDL-C the sum of atherogenic lipoproteins was calculated from the
difference of total cholesterol and HDL-cholesterol. We considered
non-HDL-C<3.3 mmol/L as the target value in chronic kidney
disease. Urinary protein, albumin and creatinine were determined
from the first morning urine. Urinary albumin was analyzed by
immunoturbidimetry, urinary total protein was measured by
turbidimetric assay. To compensate diurnal variation, first morning
urinary albumin/creatinine and protein/creatinine were taken into
consideration. Urinary and serum creatinine was determined by
kinetic Jaffe method.
In Study A during a four-year period (2009-2012) 50% of the
patients was treated with atorvastatin (10-40 mg/ day), 25% received
simvastatin (10-40 mg/ day), and 25% were treated with ezetimibe
(20-40 mg/ day).
Study B
We enrolled 21 CKD patients (19 men, 2 women); their median
Table 1: Clinical score as a basic marker of cardiovascular risk was calculated from parameters of the Framingham study [16,17].
Age (years) <40 40-60 60-70 >70
score 1 2 3 4
Hypertension
duration (years) <5 5-10 >10
<140 Hgmm 1 2 3
140-160 Hgmm 4 5 6
>160 Hgmm 7 8 9
Diabetes mellitus
duration (years) <5 5-10 >10
HbA1c= 6.5-7.5 2 4 6
HbA1c >7.5 4 6 8
Cardiac event
Acute myocardial infarction, stroke 10
Cholesterol
level (mmol/L) <4.5 4.5-5 >5
score 0 3 6
Triglyceride (mmol/L) <1.7 1.7-2.5
score 0 3
LDL-C (mmol/L) <2.5 2.5-3 >3
score 0 3 6
HDL-C (mmol/L) >1 male, >1.3 female <1 male, <1.3 female
score 0 3
Body mass index 23-25 25-30 >30
score 2 4 6
Cardiac symptoms
2 scores/symptom
chest pain
oedema
palpitation
fatigue
asphyxia
arrhythmia
cardiac
decompensation
Abbreviations: HbA1c: Hemoglobin A1c; LDL-C: Low Density Lipoprotein; HDL-C: High Density Lipoprotein
Table 2: Renal score based on GFR and proteinuria shows relative risk of cardiovascular mortality in chronic kidney disease [6,7].
Relative risk of cardiovascular mortality in
CKD on the base of GFR and proteinuria
Stages of albuminuria or proteinuria (mg/ mmol)
A1: normal
ACR <3
A2: moderate
ACR: 3-30, or
TPCR: 15-50
A3: severe
ACR >30, or
TPCR: 51-350
A3n: nephrotic
TPCR >350
GFR stages (ml/min/
1.73 m2
)
G1: normal, or elevated >90 Low Moderate High Extremely High
G2: mild decrease 60-89 Low Moderate High Extremely High
G3a: mild-moderate decrease 45-59 Moderate High Extremely High Extremely High
G3b: moderate-severe decrease 30-44 High Extremely High Extremely High Extremely High
G4: severe decrease 15-29 Extremely High Extremely High Extremely High Extremely High
G5: end-stage renal failure <15 Extremely High Extremely High Extremely High Extremely High
Low risk: 1 (relative risk: 1-1.49), moderate risk: 2 (relative risk: 1.5-2.29), high risk: 3 (relative risk: 2.3-3.69), extremely high risk: 4 (relative risk
>3.7)
ACR: urinary Albumin/Creatinine (mg/mmol), GFR: Glomerular Filtration Rate, TPCR: urinary Total Protein/Creatinine (mg/ mmol).

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age was 67 years (32-89 years). They were monitored regularly at the
Nephrology Outpatient Centre and had no previous acute cardiac
event. We enrolled patients who had complete medical history and
laboratory results to calculate clinical cardiovascular score and renal
score. Their hsTnT was determined from a fasting serum sample by
chemiluminescent immunoassay on Cobas 6000 analyzer.
Ethics approval
The work is conforming to the guiding principle of the
Declaration of Helsinki; the patients gave informed consent for the
study approved by the Institutional Committee on Human Research,
Debrecen (RKEBI/IKEBI 3764-2012).
Statistical Analysis
Statistical calculations were done using the SPSS package version
22 (IBM, Somers, NY). In the retrospective Study A we analyzed the
changes of the renal score, GFR, proteinuria and non-HDL with time
by Friedman’s test. The average yearly changes of GFR and non-HDL
demonstrated normal distribution, so one-sample t-test could be
applied to test whether the changes were significant. The change rates
of the groups with and without proteinuria were compared using two-
sample t-test. In Study B we compared troponin T levels and clinical
scores between the groups with mild vs. severe renal damage by Welch
test, since the variances of the groups were significantly different by
Levene’s test. We tested whether the troponin T level and the renal
score were independent predictors of the clinical cardiovascular score
using stepwise forward linear regression analysis.
Results
In the retrospective Study A during a four-year period (2009-
2012) we observed significant impairment of the GFR (P < 10-6
)
and renal score (P < 10-4
; Friedman test for all patients). While the
individual GFR values decreased 0-15 ml/min/1.73 m2
in a year,
urinary protein/creatinine fluctuated. During the four-year period,
considerable impairment of renal function was observed in three
patients: proteinuria increased and GFR decreased to the value of <30
ml/min/1.73 m2
. The mean of GFR decreased from 66 ± 12 to 47 ± 16
ml/min/1.73 m2
in four years. In most cases the decrease of GFR was
followed by progressing proteinuria. The clinical cardiovascular score
was proportional to the renal score: mean of clinical score was 21.8
± 9.8 at renal score <3.5 and 29.2 ± 6.7 at renal score >3.5 (p:0.09).
Our results denote that impairment of renal score based on GFR and
proteinuria indicates higher cardiovascular risk.
Efficacy of lipid lowering therapy also depended on proteinuria:
the atherogenic non-HDL-cholesterol (non-HDL-C) decreased
significantly in the 11 patients without proteinuria (P < 0.05, two-
sample t-test), but it was not reducible in the 9 patients with
proteinuria (Figure 1). Mean value of non-HDL-C decreased from
3.62 ± 0.75 to 2.92 ± 0.63 mmol/ L without proteinuria, and remained
3.5 ± 1.2 mmol/L with significant proteinuria in spite of lipid lowering
therapy (target value of non-HDL-C<3.3 mmol/ L).
In Study B (n:21) we investigated whether high sensitive Troponin
T (hsTnT) has an incremental value to predict cardiovascular risk in
CKD. Both cardiac hsTnT level (Welch test: P = 0.02) and clinical
cardiovascular score (P = 0.017) were significantly higher at severe
kidney damage (renal scores 3 or 4) than at mild kidney damage
(renal scores 1 or 2), (Figure 2). Mean of hsTnT was higher (32.8 ±
20.9 ng/L) at severe renal damage than at mild renal damage (14.8
± 11.3). The upper limit of reference range is hsTnT<14 ng/L (99
percentile value). Mean of clinical cardiovascular score was also
higher (27.4 ± 9.2) at severe renal damage than at mild renal damage
(21.5 ± 2.1), (Figure 2).
The correlation between clinical cardiovascular score and hsTnT
(R = 0.655, p < 0.001) indicates that permanent moderate elevation
of hsTnT has incremental value in predicting cardiovascular risk in
CKD (Figure 3).
Discussion
Our retrospective study detected the impairment of renal score
in a four-year period. The results support that clinical cardiovascular
score is proportional to renal score and it indicates the diagnostic
Figure 1: The efficacy of lipid lowering therapy depends on proteinuria: atherogenic non-HDL was successfully decreased in the group (n:11) without proteinuria
(P < 0.05, two-sample t-test), while change in non-HDL-C was Not Significant (NS) in patients (n:9) with proteinuria during four years long lipid lowering therapy
in Study-A.
SEE: Standard Error of the Estimate

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Figure 2: Both high sensitive troponin T (P = 0.020, Welch test) and clinical cardiovascular score (P = 0.017) were significantly higher at severe kidney damage
(renal scores 3 or 4) than at mild kidney damage (renal scores 1 or 2). Study-B, n:21.
Upper limit of the reference range is 14 ng/ L for hsTnT.
Figure 3: Clinical cardiovascular score (based on Framingham study) correlates with high sensitive troponin T level in chronic kidney disease (R = 0.655, P <
0.001). Study-B, n:21.
merit of the combined renal score for the estimation of Framingham-
based cardiovascular risk-assessment. In chronic kidney disease, for
the estimation of cardiovascular mortality risk both the glomerular
filtration rate and albumin/proteinuria should be monitored.
Permanent proteinuria alone implies an elevated cardiovascular
risk, and it indicates the progression of vascular damage. In case of
diabetes mellitus urinary albumin is recommended as a first, more
sensitive test. Even the first grade of albuminuria (3-30 mg/ mmol
urinary albumin/creatinine) indicates high risk of cardiovascular
morbidity, if GFR is decreased to as low as 45-59 ml/min/1.73 m2
(Table 2). It is in accordance with the opinion of Astor, et al. [18],
who established that 10 ml/min/1,73 m2
decrease in GFR at GFR<60
ml/min/1.73 m2
is associated with 1.29 and doubling of albuminuria
with 1.06 relative risk of cardiovascular mortality.
Among the cardiovascular lipid markers non-HDL-C decreased
in response to lipid lowering therapy only in those patients who did
not have proteinuria. The results indicate that proteinuria may be a
predictor of non-successful lipid-lowering therapy. These findings
underline the importance of monitoring proteinuria and GFR not

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only in kidney failure, but in other cardiovascular diseases as well.
One limitation of our study might be the different concentration of
the first morning urine samples, which might cause a scattering in
proteinuria, even if it was normalized to urinary creatinine. Another
limitation was the low number of cases, which was due to the fact that
to calculate Framingham clinical cardiovascular and renal scores, we
could only enroll the patients who had a complete medical history
and all laboratory results. However, the four-year follow-up proved
the utility of renal score in the estimation of cardiovascular risk.
Our results confirm that slightly elevated cardiac troponin is
common in CKD. Although a permanent slight elevation of cardiac
troponin is considered generally as a consequence of decreased
GFR [19-22], we found a moderate correlation between non-renal
clinical cardiovascular score and hsTnT. According to our results
permanently elevated troponin can be considered as a marker
of increased cardiovascular risk. Our opinion agrees with recent
publications in CKD [23-26]. If the renal score shows a rapid
impairment, it probably indicates the progression of vascular or
myocardial damage, which can be detected early by high sensitive
troponin T. Elevation of troponin depends on GFR and at end-stage
renal impairment it correlates with cardiac events and total mortality
[26]. It agrees with our opinion that in CKD hsTnT is predominantly
a marker of cardiovascular risk. Individual troponin T measured
in balanced conditions may have importance at the emergency
unit when a patient has atypical complaints and slightly elevated
troponin. For the differentiation between acute and chronic cardiac
damage, repeated troponin testing is proposed. The recent guidelines
recommended comparison of 0/1-hour or 0/3-hour values of hsTnT
with a test-specific cutoff, and it yields reliable evaluation [27,28]. The
permanent slight elevation of hsTnT can be considered as increased
cardiovascular risk. Elevated baseline troponin has an incremental
prognostic value [29] beside GFR and albumin/proteinuria in the
diagnosis and treatment of chronic kidney disease.
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